AJP - Regulatory, Integrative and Comparative Physiology, Vol 260, Issue 6 1188-R1193, Copyright © 1991 by American Physiological Society
Vasopressin and autonomic mechanisms mediate cardiovascular actions of central serotonin
P. E. Pergola and R. H. Alper
Department of Pharmacology, Toxicology, and Therapeutics, University of Kansas Medical Center, Kansas City 66103.
Intracerebroventricular administration of serotonin (5-HT) to conscious
rats increases mean arterial pressure (MAP) and decreases heart rate. To
determine the mechanisms involved, 5-HT (2.5 micrograms) was injected
intracerebroventricularly into conscious rats pretreated with various
neurotransmitter and hormone antagonists. The selective 5-HT2 antagonist LY
53857 abolished the increase in MAP and the bradycardia elicited by 5-HT.
The increase in MAP produced by 5-HT was potentiated by chlorisondamine (a
ganglionic antagonist), unaffected by prazosin (an alpha 1-antagonist) or a
vasopressin V1 antagonist alone, but eliminated by the combined
pretreatment with prazosin plus the vasopressin antagonist. In contrast,
the bradycardia was eliminated by either the vasopressin V1 antagonist or
chlorisondamine. In conclusion, 5-HT injected into the lateral cerebral
ventricle of conscious rats induces sympathoexcitation and the release of
vasopressin, which results in an increase in MAP; 5-HT also elicits a
bradycardia mediated through an interaction of the autonomic nervous system
with circulating vasopressin.
